Podcasts about cognitive deficits

People with concussions get checked out pretty thoroughly by their doctors, but for some, there are cognitive changes and deficits that doctors don't pick up.

" MANAGING COGNITIVE DEFICITS IN PERSONS LIVING WITH MENTAL HEALTH CHALLENGES (Sponsored)"

" MANAGING COGNITIVE DEFICITS IN PERSONS LIVING WITH MENTAL HEALTH CHALLENGES Pidgin (Sponsored)"

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.18.533245v1?rss=1 Authors: Sarkar, S., Gharami, K., Paidi, R. K., Srikumar, B. N., Biswas, S. C. Abstract: Astrocytes respond to any pathological insult to brain including Alzheimer's disease (AD) through 'reactive astrogliosis'. Recently, we demonstrated that tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), a neuroprotective cytokine, is released through reactive astrogliosis early in response to amyloid-{beta} (A{beta}). Here, we show that TIMP-1 has superior mechanism-of-actions on neurons in models of AD. It not only confers neuroprotection against A{beta}-induced apoptosis and autophagy via CD63 receptor but also displays synapse-specific effects that underlie cognitive recovery in AD. We detect diminished levels of TIMP-1 in the hippocampi of 5xFAD mice versus wild-type counterparts. Interestingly, exogenous TIMP-1 injection in this transgenic model ameliorates its cognitive functions, likely by restoring long-term potentiation at hippocampal synapses. We observe BDNF induction and GSK3{beta} inhibition, which may be the key TIMP-1-driven underlying mechanisms at synapses. Thus, we show an astrocyte-origin cytokine-driven mechanism for synaptic and cognitive salvation promising an exciting avenue in AD therapeutic research. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.23.529740v1?rss=1 Authors: Pradhan, A. K., Neumueller, T., Klug, C., Fuchs, S., Schlegel, M., Ballmann, M., Tartler, K. J., Pianos, A., Garcia-Sanchez, M., Liere, P., Schumacher, M., Kreutzer, M., Rupprecht, R., Rammes, G. Abstract: Alzheimer's disease (AD) is characterized by the accumulation of {beta}-amyloid peptide (A{beta}). There is increasing evidence that depression may precede AD and may be an early manifestation of dementia, suggesting common mechanisms underlying both diseases. Ligands targeting the mitochondrial translocator protein (18 kDa) (TSPO), promote neurosteroidogenesis and may be neuroprotective. Moreover, TSPO is upregulated in AD. To study whether the TSPO ligand XBD173 may exert early neuroprotective effects in AD pathology we investigated the impact of XBD173 on amyloid toxicity and neuroplasticity in mouse models. We show that XBD173 (emapunil), via neurosteroid-mediated signaling via delta subunit-containing GABAA receptors, prevents the neurotoxic effect of A{beta} on long-term potentiation (CA1-LTP) in the hippocampus and prevents the loss of spines. Chronic but not acute administration of XBD173 ameliorates spatial learning deficits in transgenic AD mice with arctic mutation (ArcA{beta}) mice. The heterozygous TSPO-knockout crossed with the transgenic arctic mutation model of AD mice (het TSPOKO X ArcA{beta}) treated with XBD173 does not show this improvement in spatial learning suggesting TSPO is needed for procognitive effects of XBD173. The neuroprotective profile of XBD173 in AD pathology is further supported by a reduction in plaques and soluble A{beta} levels in the cortex, increased synthesis of neurosteroids, rescued spine density, reduction of complement protein C1q deposits, and reduced astrocytic phagocytosis of functional synapses both in the hippocampus and cortex. Our findings suggest that XBD173 may exert therapeutic effects via TSPO in a mouse model of AD. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Yao Du is a Clinical Assistant Professor in Speech-Language Pathology at the Caruso Department of Otolaryngology-Head and Neck Surgery at the Keck School of Medicine, University of Southern California. She is a bilingual Mandarin-English speaking speech-language pathologist who has worked with pediatric and geriatric clients in schools, private practices, hospitals (inpatient and outpatient), skilled nursing facilities, and home health. She conducts research in areas of assistive technology, telepractice, and bilingualism, and also provides consulting for digital health and assistive tech startups. Deanna Hughes, PhD, CCC-SLP is a clinician and researcher who tries to improve accessibility to technology for individuals with communication disorders.Currently, she is a speech-language pathologist (SLP) with the Vista Unified School District in Vista, CA with a focus on early intervention and AAC. Claire O'Connor, B.S., is a second year speech-language pathology graduate student at Monmouth University, NJ. Her research interests include the implementation of assistive technology in communication and cognitive intervention and its efficacy on how it can be used as an effective therapeutic tool to facilitate independence among those with complex cognitive and communication needs. The virtual voice assistive technology (VAT) training is currently enrolling adults with cognitive and communication disorders (18 years old above) and caregivers to join 12-week audio and video recorded Zoom sessions, in which you will receive a FREE Amazon Echo Show device (per participant-caregiver dyad) and training on a variety of voice commands on topics such as setting reminders, selfcare/medical needs, meal preparation, news and facts, and entertainment in their daily activities. At the end of the training, our team will engage in a 1.5 hour long debrief interview where team members and caregivers will share their thoughts on the training and the device All participants are encouraged to have their family members/ caregivers present during the training. Contact us (yaodu@usc.edu) for your availability, and we look forward to enrolling you and/or your loved one. You can listen to this episode wherever you listen to podcasts or at: www.3cdigitalmedianetwork.com/telepractice-today-podcast  

References Dr Guerra EtOH lectures Dr Guerra Reward Pathway lectures Biol Psychiatry. 2020 Jan 1; 87(1): 64–73 Biochemistry and Cell Biology. 2019. Volume 97, Number 4.August. --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.16.520745v1?rss=1 Authors: Harrison, M. A. A., Morris, S. L., Rudman, G. A., Rittenhouse, D. J., Monk, C. H., Sakamuri, S. S., Jones, M. J., Hasan, M. M., Khatun, M. S., Wang, H., Garfinkel, L. P., Norton, E. B., Steele, C., Kim, S., Kolls, J. K., Jazwinski, S. M., Mostany, R., Katakam, P. V. G., Engler-Chiurazzi, E. B., Zwezdaryk, K. Abstract: Risk factors contributing to dementia are multifactorial. Pathogens as risk factors for dementia is largely correlative with few causal relationships. Here, we demonstrate that intermittent cytomegalovirus (CMV) infection in mice, mimicking human chronic infection and reactivation/reinfection events, alters blood brain barrier (BBB) metabolic pathways. An increase in basal mitochondrial function is observed in brain microvasculature endothelial cells (BMEC) at 12 months post infection but not at earlier time points and is accompanied by elevated levels of superoxide, indicative of oxidative stress. Further, these mice score lower in cognitive assays as compared to age-matched controls. Our data show that repeated systemic infection with CMV, alters BBB metabolic function and impacts cognition. These observations provide mechanistic insights through which pathogens contribute to the progression of pathologies associated with dementia. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

https://psychiatry.dev/wp-content/uploads/speaker/post-11008.mp3?cb=1669725498.mp3 Playback speed: 0.8x 1x 1.3x 1.6x 2x Download: Interventions for preventing and ameliorating cognitive deficits in adults treated with cranial irradiation – PubMed Review Matthew A Kirkman et al. CochraneFull EntryInterventions for preventing and ameliorating cognitive deficits in adults treated with cranial irradiation – PubMed

We received a question on Instagram about what sensory strategies we would recommend to help a child who has lower cognitive abilities or who is non-speaking or pre-verbal.We've had many, many clients who had learning disabilities, used AAC devices because they didn't communicate verbally, or who struggled overall with communication - expressive and receptive. In this episode, we're going to draw from our own personal experiences as well as research! Be sure to check out the show notes on our blog at  Harkla.Co/Podcast.Brought To You By HarklaThis podcast is brought to you by Harkla.  Our mission at Harkla is to help those with special needs live happy and healthy lives. We accomplish this through high-quality sensory products & child development courses.Podcast listeners get 10% off their first order at Harkla with the discount code "sensory". Head to Harkla.co/sensory to start shopping now.LinksLooking for more in-depth help? Sign up for 2-on-1 Mentoring With Us!!FREEBIES!All Things Sensory Podcast Instagram Harkla YouTube ChannelHarkla Website Harkla InstagramEp. 25 Executive Functioning Ep. 107 Interactive Metronome Ep. 139 Incorporating Speech into Play YouTube - Build an Obstacle CourseWhat are Cognitive Deficits?Clinical Characteristics of Intellectual DisabilitiesEncyclopedia of ASD - Preverbal CommunicationEffects of Vestibular Stimulation on Spontaneous Use of Verbal Language The Immediate Effects of Vestibular Stimulation on Language PerformanceThe Beneficial Effect of Vestibular StimulationHappy Hug Sensory Tube Interactive Metronome Homedics Pure Therapy Head Massager 

Dr. Richard S.E. Keefe (Duke University Medical Center, Durham, North Carolina) discusses an article looking at an intervention for major depressive disorder that takes the form of a videogame. Afterwards, AJP Editor-in-Chief Dr. Ned Kalin discusses the July issue's theme. Keefe interview: [01:00] What were your results? [03:13] What do videogames offer as a depression intervention? [03:43] Differences between the intervention and the control intervention [05:05] What was the impact of the interventions? [06:51] What were the limitations of the design and what might change going forward? [08:10] Does the patient's perception of the effectiveness of the intervention matter? [09:20] How the intervention differs from a similar intervention aimed at children [10:19] Is there an advantage to “hiding” the intervention as a videogame? [11:33] Designing a game and an intervention that work simultaneously [13:27] What next for your research? [15:05] Kalin interview [16:11] Keefe et al. [16:22] Tabuteau et al. [18:15] Ge et al. [20:54] Pan et al. [22:01] Tamm et al. [23:47] Pizzagalli [25:30] Grogans et al. [26:02] Be sure to let your colleagues know about the podcast, and please rate and review it on Apple Podcasts, Google Podcasts, Stitcher, Spotify, or wherever you listen to it. Subscribe to the podcast here. Listen to other podcasts produced by the American Psychiatric Association. Browse articles online. Watch Deputy Editor Daniel S. Pine, M.D., present highlights from the May 2021 issue. How authors may submit their work. Follow the journals of APA Publishing on Twitter. E-mail us at ajp@psych.org

Fast Takes - Episode 42 In this episode, Brian Sandroff, PhD, senior research scientist in the Center for Neuropsychology and Neuroscience Research at Kessler Foundation, talks about his peer-reviewed article, “Developing the Rationale for Including Virtual Reality in Cognitive Rehabilitation and Exercise Training Approaches for Managing Cognitive Dysfunction in MS,” published in April 2022, in the journal NeuroSci. He discusses how virtual reality could increase sensory input and promote multisensory integration and processing during rehabilitation for multiple sclerosis. Learn more about: 
Dr. Brian Sandroff, https://kesslerfoundation.org/about-us/foundation-staff/brian-m-sandroff-phd Center for Neuropsychology and Neuroscience Research, https://kesslerfoundation.org/center-neuropsychology-and-neuroscience-research The peer-reviewed article at www.mdpi.com/2673-4087/3/2/15 Co-authors: Carly L. A. Wender, https://kesslerfoundation.org/about-us/foundation-staff/carly-wender, John DeLuca, https://kesslerfoundation.org/aboutus/John%20DeLuca, Brian M. Sandroff ======================================================= Tuned in to our podcast series lately? Join our listeners in 90 countries who enjoy learning about the work of Kessler Foundation. Be sure to subscribe to our SoundCloud channel “KesslerFoundation” for more research updates. 
Follow us on Facebook, Twitter, and Instagram. Listen to us on Apple Podcasts, Spotify, SoundCloud, or wherever you get your podcasts. This podcast was recorded remotely on May 4, 2022, and was edited and produced by Joan Banks-Smith, Creative Producer for Kessler Foundation.

In this episode, Ayesha discussed a presentation at this year's Alzheimer's Association International Conference (AAIC) 2021 about the impacts of COVID-19 on cognitive health. The study, conducted at New York University Langone Health, found that in cognitively normal COVID-19 patients that experienced the neurological symptom of confusion due to toxic-metabolic encephalopathy (TME), levels of serum biomarkers associated with neuroinflammation, neuronal injury and Alzheimer's disease (such as phosphorylated Tau 181 and neurofilament light protein) were higher than in patients that did not have TME. The strong correlation of these serum biomarkers with the presence of neurological symptoms in COVID-19 patients suggest that COVID-19 patients could experience an acceleration of AD/ADRD symptoms and pathology.Ayesha also discussed another story about serum biomarkers for the early detection of pancreatic cancer. Immunovia, a Swedish biotech firm, has developed a nine-panel biomarker blood test that can be used for the detection of pancreatic in early stages. The company's American subsidiary, located in Massachusetts, received approval for the test early this month and the Massachusetts Department of Public Health has already begun using it to test patients for the deadly cancer. The test evaluates a combination of immunoregulatory and tumor biomarkers. Early detection of pancreatic cancer is a significant unmet clinical need because the cancer is typically diagnosed in late stages when treatment options are limited and the disease is difficult to treat.AAIC 2021: Insights into COVID-19 Impacts on Cognitive HealthImmunovia's Pancreatic Cancer Blood Test is World's First for Early Disease DetectionFor more life science and medical device content, visit the Xtalks Vitals homepage.Follow Us on Social MediaTwitter: @Xtalks Instagram: @Xtalks Facebook: https://www.facebook.com/Xtalks.Webinars/ LinkedIn: https://www.linkedin.com/company/xtalks-webconferences YouTube: https://www.youtube.com/c/XtalksWebinars/featured

Shawn Weiss talks about fall prevention during the pandemic. Shawn is a member of the Ohio Falls Coalition and Ohio Injury Prevention Partnership, has been a physical therapist for 23 years, and is published in Fall Prevention for Residents with Cognitive Deficits residing in Assisted Living Facilities. She talks about why there has been a rising number of falls and fall-related injuries in the aging population during the COVID-19 pandemic, how we can help senior loved ones whose health may have declined during the pandemic, and provides some community resources to seek out.

Resources mentioned during this episode:Performance Assessment of Self-Care SkillsCognitive Disorders Fact SheetFunctional Cognition and OT (Book)

Fast Takes – Episode 10 View the transcript at https://kesslerfoundation.org/sites/default/files/2021-01/Patterns%20of%20cognitive%20deficits%20in%20persons%20with%20spinal%20cord%20injury%20as%20compared%20with%20both%20age-matched%20and%20older%20individuals%20without%20sci-TRANSCRIPT.pdf In this episode, Trevor Dyson-Hudson, MD, Director for the Center for Spinal Cord Injury Research and the Center for Outcomes and Assessment Research at Kessler Foundation talks about his latest peer reviewed article “Patterns of cognitive deficits in persons with spinal cord injury as compared with both age-matched and older individuals without spinal cord injury” published in the Journal of Spinal Cord Medicine online December 3, 2018. Funding Source: New Jersey Commission on Spinal Cord Research and Rehabilitation Research and Development Service Read more about Dr. Dyson-Hudson and his research at https://kesslerfoundation.org/aboutus/Trevor%20Dyson-Hudson For more information about this study, check out the press release at https://www.eurekalert.org/pub_releases/2019-01/kf-ris011819.php or at https://doi.org/10.1080/10790268.2018.1543103 Co-authors: Nancy D. Chiaravalloti, PhD, Erica Weber, PhD, Glenn Wylie, DPhil, and Trevor Dyson-Hudson, MD, from Kessler Foundation, and Jill M. Wecht, EdD, from the James J. Peters VA Medical Center Follow us on Facebook, Twitter, and Instagram. Listen to us on Apple Podcasts, Spotify, SoundCloud, or wherever you get your podcasts. This podcast was recorded on Monday, September 24, 2020 remotely and was edited and produced by Joan Banks-Smith, Creative Producer for Kessler Foundation.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.31.229583v1?rss=1 Authors: Koren, S. A., Hamm, M. J., Cloyd, R., Fontaine, S. N., Chishti, E., Lanzillotta, C., Di Domenico, F., Seyfried, N., Duong, D., Powell, D. K., Vandsburger, M., Hartz, A. M. S., Koren, J., Axten, J. M., Laping, N. J., Abisambra, J. F. Abstract: Tauopathies are a group of more than twenty known disorders that involve progressive neurodegeneration, cognitive decline, and pathological tau accumulation. Current therapeutic strategies provide only limited, late-stage symptomatic treatment. This is partly due to lack of understanding of the molecular mechanisms linking tau and cellular dysfunction, especially during the early stages of disease progression. In this study, we treated early stage tau transgenic mice with a multi-target kinase inhibitor to identify novel substrates that contribute to cognitive impairment and exhibit therapeutic potential. Drug treatment significantly ameliorated brain atrophy and cognitive function as determined by behavioral testing and a sensitive imaging technique called manganese-enhanced magnetic resonance imaging (MEMRI) with quantitative R1 mapping. Surprisingly, these benefits occurred despite unchanged hyperphosphorylated tau levels. To elucidate the mechanism behind these improved cognitive outcomes, we performed quantitative proteomics to determine the altered protein network during this early stage in tauopathy and compare this model with the human AD proteome. We identified a cluster of preserved pathways shared with human tauopathy with striking potential for broad multi-target kinase intervention. We further report high confidence candidate proteins as novel therapeutically relevant targets for the treatment of tauopathy. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.24.220129v1?rss=1 Authors: Wang, S., Leem, J., Podvin, S., Hook, V., Kleschevnikov, N., Savchenko, P., Dhanani, M., Zhou, K., Kelly, I., Zhang, T., Miyanohara, A., Kleschevnikov, A., Wagner, S., Trojanowski, J., Roth, D., Patel, H., Patel, P., Head, B. P. Abstract: AD presents with severe neurodegeneration which leads to cognitive deficits and dementia. Identifying the molecular signals that attenuate neurodegeneration in AD may be exploited as therapeutic targets. This study revealed that transgenic AD mice (PSAPP) exhibit decreased caveolin-1 (Cav-1), a membrane/lipid raft (MLR) scaffolding protein that organizes synaptic signaling components. Subcellularly, Cav-1 and full length (fl)-TrkB were significantly decreased in MLRs. We thus developed an in vivo gene therapy that re-expresses neuronal-targeted Cav-1 using the synapsin promoter (SynCav1). While AD mice showed significant learning and memory deficits at 9 and 11 months, AD mice that received hippocampal SynCav1 (AD-SynCav1) maintained normal learning and memory at 9 and 11 months respectively. Furthermore, AD-SynCav1 mice showed preserved hippocampal MLR-localized fl-TrkB, synaptic ultrastructure, dendritic arborization and axonal myelin content, all of which occurred independent of reducing amyloid deposit and astrogliosis. Thus, SynCav1 demonstrates translational potential to treat AD by delaying neurodegeneration. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.13.200519v1?rss=1 Authors: Meinhardt, M. W., Pfarr, S., Rohleder, C., Vengeliene, V., Barroso-Flores, J., Hoffmann, R., Meinhardt, M. L., Paul, E., Hansson, A. C., Köhr, G., Meier, N., von Bohlen und Halbach, O., Bell, R. L., Endepols, H., Neumaier, B., Schönig, K., Bartsch, D., Spanagel, R., Sommer, W. H. Abstract: Alcohol-dependent patients commonly show impairments in executive functions that facilitate craving and can lead to relapse. The medial prefrontal cortex, a key brain region for executive control, is prone to alcohol-induced neuroadaptations. However, the molecular mechanisms leading to executive dysfunction in alcoholism are poorly understood. Here using a bi-directional neuromodulation approach we demonstrate a causal link for reduced prefrontal mGluR2 function and both impaired executive control and alcohol craving. By neuron-specific prefrontal knockdown of mGluR2 in rats, we generated a phenotype of reduced cognitive flexibility and excessive alcohol-seeking. Conversely, restoring prefrontal mGluR2 levels in alcohol-dependent rats rescued these pathological behaviors. Also targeting mGluR2 pharmacologically reduced relapse behavior. Finally, we developed a FDG-PET biomarker to identify those individuals that respond to mGluR2-based interventions. In conclusion, we identified a common molecular pathological mechanism for both executive dysfunction and alcohol craving, and provide a personalized mGluR2-mechanism-based intervention strategy for medication development of alcoholism. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.09.141754v1?rss=1 Authors: Sarkar, T., Patro, N., Patro, I. Abstract: Perinatal protein malnourishment is a leading cause for mental and physical retardation in children with poor socioeconomic conditions. Such malnourished children are vulnerable to additional stressors, that may synergistically act to cause neurological disorders at adulthood. In this study, the above mentioned condition is mimicked via a multi-hit rat model in which pups born to protein malnourished mothers (LP) were co-injected with polyinosinic:polycytidylic acid (Poly I:C; viral mimetic) at Postnatal day (PND) 3 and lipopolysaccharide (LPS; bacterial mimetic) at PND 9. Individual exposure of Poly I:C and LPS was also given to LP pups to correlate chronicity of stress. Similar treatments were also given to control pups. Hippocampal cellular apoptosis, {beta} III tubulin catastrophe, altered neuronal profiling and spatial memory impairments were assessed at PND 180, using specific immunohistochemical markers (active caspase 3, {beta} III tubulin, doublecortin), Golgi studies and cognitive mazes (Morris Water Maze and T maze). Increase in cellular apoptosis, loss of dendritic arborization and spatial memory impairments were higher in multi-hit group, than the single-hit groups. Such impairments observed due to multi-hit stress, mimic conditions similar to many neurological disorders and hence it is hypothesized that later life neurological disorders might be an outcome of multiple early life hits. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.01.064576v1?rss=1 Authors: Savard, M., Pascoal, T., Dhollander, T., Iturria-Medina, Y., Vitali, P., Therriault, J., Mathotaarachchi, S., Benedet, A. L., Gauthier, S., Rosa Neto, P. Abstract: Fronto-temporal dementia (FTD) is a neurodegenerative disease characterized by focal atrophy of the gray matter (GM), especially in the frontal and temporal regions. Recent studies suggest a framework where white matter (WM) atrophy plays an important role in FTD pathophysiology. However, these studies often overlook the fact that WM tracts bridging different brain regions may have different vulnerabilities to the disease and the relative contribution of GM atrophy to this WM model, resulting in a less comprehensive understanding of the relationship between clinical symptoms and pathology. Here, by leveraging the sensitivity of advanced diffusion MRI modelling and metrics to precise white matter microstructural properties, we aim to clarify the relative contributions of WM fibers and GM atrophy to the cognitive symptoms typically found in FTD. A total of 155 participant from the Frontotemporal Lobar Degeneration Neuroimaging Initiative (FTLDNI) were analysed, including 68 normal elderly controls (CN), 28 behavioral variants (BV), 26 sematic variants (SV) and 30 progressive non fluent aphasia variants (PNFA) of FTD. Diffusion MRI analysis was performed using two complementary techniques: whole brain fixel-based analysis (FBA) and structural connectivity based on probabilistic tractography. Whole brain GM atrophy was assessed using voxel-based morphometry (VBM). Using a common factor analysis to extract a semantic and an executive factor, we aim to test the relative contribution of WM and GM of specific tracts in predicting cognition. We found that semantic symptoms were mainly dependent on short-range WM fiber disruption, while damage to long-range WM fibers was preferentially associated to executive dysfunction with the GM contribution to cognition being predominant for local processing. Our results support the importance of the disruption of specific WM tracts to the core cognitive symptoms associated with FTD. As large-scale WM tracts, which are particularly vulnerable to vascular disease, were highly associated with executive dysfunction, our findings highlight the importance of controlling for risk factors associated with deep white matter disease, such as vascular risk factors, in patients with FTD in order not to potentiate underlying executive dysfunction. Copy rights belong to original authors. Visit the link for more info

Neurocognitive deficits are commonly experienced by individuals living with bipolar disorder. Bipolar disorder is known to affect attention, processing speed, verbal learning and memory, and executive functions, including working memory and verbal fluency. During this webinar, Dr. Roger S. McIntyre discusses cognitive dysfunction in adults with bipolar disorder and associated health implications; underlying mechanisms that may contribute to cognitive dysfunction; and the importance of preserving cognitive function in this population. Roger S. McIntyre, M.D., FRCPC, is a Professor of Psychiatry & Pharmacology at the University of Toronto. He also serves as Head of the Mood Disorders Psychopharmacology Unit University Health Network, and Executive Director of the Brain & Cognition Discovery Foundation. He received his medical degree at Dalhousie University and completed his psychiatry residency at the University of Toronto. Disclaimers Speaker is a paid consultant of Otsuka Pharmaceutical Development & Commercialization, Inc. PsychU is supported by Otsuka Pharmaceutical Development & Commercialization, Inc. (OPDC), Otsuka America Pharmaceutical, Inc. (OAPI), and Lundbeck, LLC – committed supporters of the mental health treatment community. The opinions expressed by PsychU’s contributors are their own and are not endorsed or recommended by PsychU or its sponsors. The information provided through PsychU is intended for the educational benefit of mental health care professionals and others who support mental health care. It is not intended as, nor is it a substitute for, medical care, advice, or professional diagnosis. Health care professionals should use their independent medical judgement when reviewing PsychU's educational resources. Users seeking medical advice should consult with a health care professional. No CME or CEU credits are available through any of the resources provided by PsychU. Some of the contributors may be paid consultants for OPDC, OAPI, and / or Lundbeck, LLC. MRC2.CORP.X.03556 / MRC2.CORP.X.03556

Is brain damage the only cause of problems identified on neuropsychological testing? What else may be causing or contributing to deficits?   Interview with Neuropsychologist Arnold Purisch, PhD  Dr. Dan Gardner's YouTube and Podcast channels and his website do NOT offer medical advice. You should not rely on this information as a substitute for, nor does it replace, professional medical advice, diagnosis, or treatment. See full Disclaimer: http://bit.ly/dgdisclaimer **SUBSCRIBE FOR VIDEOS ** *Interviews of brain injury survivors, family, and healthcare treaters *Your Peripheral Brain (assistive technology tips)* SUBSCRIBE TO VIDEOS http://bit.ly/tbirecovery-subscribe **SUBSCRIBE TO PODCAST** https://dangardner.podbean.com/ **SUBSCRIBE TO NEWSLETTERS** Traumatic Brain Injury Recovery Updates http://bit.ly/tbiupdates Your Peripheral Brain - Assistive Tech Updates http://bit.ly/dgtechtips  

02:14 – John’s Superpower: Talking About Feelings in Public 04:57 – Programmers and Feelings Coraline Ada Ehmke: Emotions as State Machines (https://www.greaterthancode.com/2017/07/12/emotions-as-state-machines/) 09:39 – Being Educated About Your Emotions https://pbs.twimg.com/media/DcSyorTUwAA5UOx.jpg image via https://pbs.twimg.com/media/DcSyorTUwAA5UOx.jpg 16:12 – Feelings As Addictions, Comparing Your Experiences to Others’ Experiences, and Setting Boundaries 24:05 – Emotional API 28:53 – Cognitive Deficits of Not Handling Emotions and Cognitive Benefits of Developing Fluency with Emotions Analysis Paralysis (https://en.wikipedia.org/wiki/Analysis_paralysis) 34:02 – Doing Work to Understand Your Emotions “Practice doesn’t make perfect; practice makes permanent.” ~ Katrina Owen 36:34 – Getting Paid/Getting Further for Having and Learning About Emotional Intelligence 41:18 – Negative Effects on Teams When Individuals Refuse to Acknowledge Emotions 43:59 – Influencing Emotions and Emotional Responses Dialectical Behavior Therapy (https://en.wikipedia.org/wiki/Dialectical_behavior_therapy) TIP: Temperature Change, Intense Exercise, Progressive Relaxation (https://peerguideddbtlessons.weebly.com/tip-skills.html) This episode was brought to you by @therubyrep (https://twitter.com/therubyrep) of DevReps, LLC (http://www.devreps.com/). To pledge your support and to join our awesome Slack community, visit patreon.com/greaterthancode (https://www.patreon.com/greaterthancode). To make a one-time donation so that we can continue to bring you more content and transcripts like this, please do so at paypal.me/devreps (https://www.paypal.me/devreps). You will also get an invitation to our Slack community this way as well. Amazon links may be affiliate links, which means you’re supporting the show when you purchase our recommendations. Thanks!

Prevalence & Nature of Cognitive Deficits in MS presented by Dr. John DeLuca Welcome to Kessler Foundations 2017 Multiple Sclerosis consumer conference, Improving Cognitive, Emotional, & Physical Health in Multiple Sclerosis This conference is hosted by Kessler Foundation and is being funded by the National Multiple Sclerosis Society (Grant #1508-05940) Our first session of the conference: Prevalence & Nature of Cognitive Deficits in MS was presented by Dr. John DeLuca. Dr. DeLuca is internationally known for his work on cognitive processing, cognitive rehabilitation, neuroimaging, and fatigue in neurological populations. He is senior vice president for Research and Training at Kessler Foundation. This presentation was recorded and produced by Joan Banks-Smith, Creative Producer for Kessler Foundation on Friday, October 13, 2017 at the The Westminster Hotel, 550 W. Mt. Pleasant Avenue,Livingston, New Jersey 07039 Be sure and check out all of the conference podcast presentation at KesslerFoundation.org/MS2017 and slides at kesslerfoundation.org/podcastpdf For more information about our research, go to KesslerFoundation.org

Staying Cognitively Active presented by Dr. John DeLuca Welcome to Kessler Foundations 2017 Multiple Sclerosis consumer conference, Improving Cognitive, Emotional, & Physical Health in Multiple Sclerosis This conference is hosted by Kessler Foundation and is being funded by the National Multiple Sclerosis Society (Grant #1508-05940) Our first session of the conference: Prevalence & Nature of Cognitive Deficits in MS was presented by Dr. John DeLuca. Dr. DeLuca is internationally known for his work on cognitive processing, cognitive rehabilitation, neuroimaging, and fatigue in neurological populations. He is senior vice president for Research and Training at Kessler Foundation. This presentation was recorded and produced by Joan Banks-Smith, Creative Producer for Kessler Foundation on Friday, October 13, 2017 at the The Westminster Hotel, 550 W. Mt. Pleasant Avenue,Livingston, New Jersey 07039 Be sure and check out all of the conference podcast presentation at KesslerFoundation.org/MS2017 and slides at kesslerfoundation.org/podcastpdf For more information about our research, go to KesslerFoundation.org

Host: Paul Rokuskie Social and emotional skills come fairly easily for neurotypical individuals. But for those with a diagnosis of Autism Spectrum Disorder (ASD), these may be some of the most challenging skills to learn. Thankfully there is a lot of experience among educators using techniques to help individuals with ASD become more social. Join host Paul Rokuskie as he welcomes speech/language pathologist Jill Kuzma to discuss therapeutic approaches for social cognitive deficits in children with ASD.

Cognitive impairment after stroke is common and can cause disability with major impacts on quality of life and independence. There are also indirect effects of cognitive impairment on functional recovery after stroke through reduced participation in rehabilitation and poor adherence to treatment guidelines. In this article, we attempt to establish the following: ● whether there is a distinct profile of cognitive impairment after stroke; ● whether the type of cognitive deficit can be associated with the features of stroke-related damage; and ● whether interventions can improve poststroke cognitive performance. There is not a consistent profile of cognitive deficits in stroke, though slowed information processing and executive dysfunction tend to predominate. Our understanding of structure–function relationships has been advanced using imaging techniques such as lesion mapping and will be further enhanced through better characterization of damage to functional networks and identification of subtle white matter abnormalities. Effective cognitive rehabilitation approaches have been reported for focal cortical deficits such as neglect and aphasia, but treatments for more diffusely represented cognitive impairment remain elusive. In the future, the hope is that different techniques that have been shown to promote neural plasticity (e.g., exercise, brain stimulation, and pharmacological agents) can be applied to improve the cognitive function of stroke survivors.

"Fatigue and Cognitive Deficits in Depression" was given by Paola Pedrelli at The 4th Annual Massachusetts General Hospital Colloquium on Depression in Boston, Massachusetts on June 2nd, 2012.

"Fatigue and Cognitive Deficits in Depression" was given by Paola Pedrelli at The 4th Annual Massachusetts General Hospital Colloquium on Depression in Boston, Massachusetts on June 2nd, 2012.

Wed, 19 Oct 2011 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/13447/ https://edoc.ub.uni-muenchen.de/13447/2/Wang_Xiao-Dong.pdf Wang, Xiao-Dong

Tue, 14 Dec 2010 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/12541/ https://edoc.ub.uni-muenchen.de/12541/1/Knapman_Alana_Thesis.pdf Knapman, Alana

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.15.043570v1?rss=1 Authors: Phensy, A. J., Lindquist, K., Lindquist, K., Bairuty, D., Gauba, E., Guo, L., Tian, J., Du, H., Kroener, S. Abstract: Redox dysregulation and oxidative stress are final common pathways in the pathophysiology of a variety of psychiatric disorders, including schizophrenia. Oxidative stress causes dysfunction of GABAergic parvalbumin-positive interneurons (PVI), which are crucial for the coordination of neuronal synchrony during sensory- and cognitive-processing. Mitochondria are the main source of reactive oxygen species (ROS) in neurons and they control synaptic activity through their roles in energy production and intracellular calcium homeostasis. We have previously shown that in male mice transient blockade of NMDA receptors during development (subcutaneous injections of 30 mg/kg ketamine (KET) on postnatal days 7, 9, and 11) results in long-lasting alterations in synaptic transmission and reduced parvalbumin expression in the adult prefrontal cortex (PFC), contributing to a behavioral phenotype that mimics multiple symptoms associated with schizophrenia. These changes correlate with oxidative stress and impaired mitochondrial function in both PVI and pyramidal cells. Here, we show that genetic deletion (Ppif-/-) of the mitochondrial matrix protein cyclophilin D (CypD) prevents perinatal KET-induced increases in ROS and the resulting deficits in PVI function, and changes in excitatory and inhibitory synaptic transmission in the PFC. Deletion of CypD also prevented KET-induced behavioral deficits in cognitive flexibility, social interaction, and novel object recognition. Taken together, these data highlight how mitochondrial activity may play an integral role in modulating PVI-mediated cognitive processes. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.22.055459v1?rss=1 Authors: Anandarajah, H., Seitzman, B. A., McMichael, A., Dworetsky, A., Coalson, R. S., Jiang, C., Gu, H., Barbour, D. L., Schlaggar, B. L., Limbrick, D. D., Rubin, J. B., Shimony, J. S., Perkins, S. M. Abstract: Pediatric brain tumor survivors experience significant cognitive sequelae from their diagnosis and treatment. The exact mechanisms of these injuries are poorly understood, and validated predictors of cognitive outcome are lacking. The current study aims to determine if there are abnormalities in functional brain network organization and cognitive performance in pediatric brain tumor patients, measured via resting state functional magnetic resonance imaging (rsfMRI) and the NIH Toolbox Cognition Battery, respectively. Further, we assess potential relationships between changes in brain network architecture and behavior in the patients. Patients ages 4-18 years old with diagnosis of a brain tumor underwent awake rsfMRI during regularly scheduled clinical imaging and were tested with the NIH Toolbox Cognition Battery. Overall, functional brain network organization was significantly different in patients compared to age- and sex-matched healthy controls (p < 0.001). Network integrity within the dorsal attention network was particularly affected, with 86% of patients having connectivity strength 2+ SD below the mean of controls (p < 0.0001). Moreover, cognitive testing of patients demonstrated significant impairments in multiple domains, including attention (p < 0.05, FDR corrected). Finally, a significant amount of variance of age-adjusted total composite scores from the Toolbox was explained by changes in segregation between the dorsal attention and default mode networks as well as sex (R2 = 0.52, p < 0.05). Pediatric brain tumor patients demonstrated statistically significant deficits in multiple cognitive domains and multiple abnormalities in brain network architecture. Thus, rsfMRI may provide insight into neural systems that underlie these changes in cognitive function, suggesting that these metrics may serve as a biomarker for cognitive performance. Copy rights belong to original authors. Visit the link for more info